How to deal with GLAUCOMA with clinical

How to deal with GLAUCOMA with clinical


  • Glaucoma is not a single disease process but a group of disorders characterized by a progressive optic neuropathy resulting in a characteristic appearance of the optic disc and a specific pattern of irreversible visual field defects that are associated frequently but not invariably with raised intraocular pressure (IOP).


Clinico-etiologically glaucoma may be classified as follows:

  1. Congenital/Developmental Glaucomas
  2. Primary congenital glaucoma (without associated anomalies).
  3. Developmental glaucoma (with associated anomalies).
  4. Primary Adult Glaucomas
  5. Primary open-angle glaucomas (POAG)
  6. Primary angle-closure glaucoma (PACG)
  7. Primary mixed mechanism glaucoma
  8. Secondary Glaucomas




  • Chronic simple glaucoma


  • It is a type of primary glaucoma, where there is no obvious systemic or ocular cause of rise in the intraocular pressure.


  1. Slowly progressive raised intraocular pressure (>21 mm Hg recorded on at least few occasions) associated with
  2. Open normal appearing anterior chamber angle
  3. Characteristic optic disc cupping
  4. Specific visual field defects.



  1. Intraocular pressure (IOP)
  2. Hereditary
  3. Age : Elders b/w 50-70 years.
  4. Race : More in blacks than in whites
  5. Myopes
  6. Diabetics
  7. Cigarette smoking
  8. High BP


Thickening and sclerosis of trabecular meshwork with faulty collagen tissue

Narrowing of intertrabecular spaces

Deposition of amorphous material in the juxtacanalicular space

Collapse of Schlemm’s canal and absence of giant vacuoles in the cells lining it


  2. Slowly progressive and usually asymptomatic.
  3. Mild headache and earache
  4. Difficulty in reading and close work
  5. Delayed work adaptation
  6. Significant vision loss and blindness
  1. Anterior segment signs
  1. Ocular examination including slit-lamp biomicroscopy may reveal normal anterior segment.
  2. In late stages, pupil reflex becomes sluggish and cornea may show slight haze.
  • IOP changes
  1. In the initial stages, the IOP may not be raised permanently, but there is an exaggeration of the normal diurnal variation.
  2. Therefore, repeated observations of IOP (every 3–4 hour), for 24 hours is required during this stage (Diurnal variation test).
  3. A variation in IOP of over 5 mm Hg (Schiotz) is suspicious and over 8 mm of Hg is diagnostic of glaucoma.
  4. In later stages, IOP is permanently raised above 21 mm of Hg and ranges between 30 and 45 mm of Hg.
  • Cupping of the optic disc
  1. A slowly progressive cupping of the optic disc is an essential feature of POAG. Normal cup disc ratio 0.3  .
  2. Glaucomatous cupping of the cup has following features :
  3. Vertically oval cup due to selective loss of neural rim tissue in the inferior and superior poles.
  4. Asymmetry of the cups: A difference of more than 0.2 between two eyes is significant.
  5. Large cup, i.e., 0.6 or more (normal cup size is 0.3 to 0.4) may occur due to concentric expansion.
  6. Splinter haemorrhages present on or near the optic disc margin.
  7. Pallor areas on the disc.
  8. Nasal shift of blood vessels at the disc.
  9. Marked cupping may occur in advanced cases.
  10. Glaucomatous optic atrophy white and deep excavated disc is the end result.
  • Visual field defects
  1. Baring of blind spot
  2. Small wing-shaped paracentral scotoma
  3. Sickle-shaped extension of blind spot known as Seidel’s scotoma
  4. Arcuate or Bjerrum’s scotoma
  5. Ring or double arcuate scotoma
  6. Roenne’s central nasal step
  7. Peripheral field defects
  8. Tubular vision with a temporal island of vision
  9. Advanced field loss with a temporal island of vision only
  10. Complete vision loss


  1. Tonometry
  2. Central corneal thickness (CCT)
  3. Diurnal variation test
  4. Gonioscopy
  5. Documentation of optic disc changes
  6. Slit-lamp examination of anterior segment
  7. Perimetry
  8. Nerve fibre layer analyzer (NFLA)
  9.  Provocative tests


  2. Characteristically POAG is labelled when raised IOP (>21 mm of Hg) is associated with definite glaucomatous optic disc cupping and visual field changes.
  • When a patient has an IOP constantly more than 21 mm of Hg but no optic disc and visual field changes.
  • When typical glaucomatous disc cupping with or without visual field changes is associated with an intraocular pressure constantly below 21 mm of Hg.


  1. Medical Therapy
Topical beta –blockers  Timolol maleate 0.25%, 0.5%1-2 times a day
Betaxalol 0.25%2 times a day
Levobunolol 0.25%, 0.5%1-2 times a day
Pilocarpine 1,2,4%————-3-4 times a day
Dorzolamide 2%————-2-3 times a day
Latanoprost 0.0005%————-2-3 times a day
Adrenergic drugsEpinephrine hydrochloride 0.5, 1.25%1-2 times a day
Dipivefrine 0.1%1-2 times a day
  • Argon or Diode Laser Trabeculoplasty
  • Filtration Surgery


  1. Uncontrolled glaucoma despite maximal medical therapy and laser trabeculoplasty.
  2. Noncompliance of medical therapy and non- availability of ALT/SLT.
  3. Failure of medical therapy and unsuitable for ALT either due to lack of cooperation or inability to visualize the trabeculum.
  4. Eyes with advanced disease, i.e., having very high IOP, advanced cupping and advanced field loss should be treated with filtration surgery as primary line of management.

Types of surgery

  1. Fistulizing (filtration) surgery which provides a new channel for aqueous outflow and successfully controls the IOP (below 21 mm of Hg).
  2. Trabeculectomy is the most frequently performed filtration surgery nowadays.


  • In this there is a sudden rise of IOP due to blockage of the aqueous outflow by closure of a narrow angle of the anterior chamber.


  1. Predisposing factors
  2. Age : 50-60 years
  3. Sex: more in females ( 1:4)
  4. Race : more in south east Asians and eskimos and uncommon in blacks
  5. Hypermetropic eyes with shallow anterior chamber and short axial length.
  6. Eyes in which iris-lens diaphragm is placed anteriorly.
  7. Eyes with narrow angle of anterior chamber, which may be due to small eyeball.
  8. Plateau iris configuration
  1. Precipitating factors
  1. Dim illumination
  2. Emotional stress
  3. Use of mydriatics


Mid dilated pupil

Increased contact b/w lens and iris

Relative pupil block

Physiological iris bombe

Appositional angle closure

Synechial angle closure

Prolonged rise in IOP


    PRODROMAL STAGE (LATENT GLAUCOMA )Intermittent attacks of transient rise in IOP.Blurring of visionColoured halos around light and mild headacheProne dark-room provocative test ( +ve if 8mm of Hg rise occurs in one hour )Laser IridotomySurgical Peripheral Iridectomy
    PHASE OF CONSTANT INSTABILITY ( INTERMITTENT OR SUBACUTE GLAUCOMA )Attacks of rise of IOP become more frequent and each attack lasts for few mins. to 1-2 hours.**Above signs are added.**Prone dark-room provocative testLaser IridotomySurgical Peripheral Iridectomy   *Should be done after medical control of IOP*
    ACUTE ANGLE CLOSURE GLAUCOMA ( ACUTE CONGESTIVE GLAUCOMA )Sudden rise in IOP occurs due to total angle closure.SYMPTOMSSudden onset of Pain.Nausea, vomiting and prostrations are frequently associated with pain. Rapidly progressive impairment of vision, redness, photophobia and lacrimation develop in all cases.SIGNSLid oedemaCiliary and conjunctival congestionCorneal oedemaMid dilated vertically over pupilShallow anterior chamberIris discolorationStromal oedemaRaised IOPClosed angle of anterior chamberMEDICAL T/TAcetazolamide – 500mg stat nad then 250 mg qidGlycerol 1-2 kg per body weight orally in lemon juiceMannitol 1-2 kg per body weight given IV over 30 mins. Pilocarpine 2-4% every 15 mins. for 1 hour and then qidTopical steroids 3-4 times a dayAnalgesics   SURGICAL T/TPeripheral Iridectomy / Laser Iridotomy Filtration Surgery ( Trabeculectomy )

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